【Animal Modeling】-Characteristics of cardiac structure and function pathological process in a mouse model of pressure overload heart failure

  Objective To establish a mouse model of heart failure, and to comprehensively evaluate the characteristic changes of cardiac function and structure during the development of the disease by using ultrasound imaging and pathological techniques.

  Methods Aortic arch coarctation was used to establish a pressure overload-induced heart failure model in mice. The blood flow Doppler at the coarctation of the aortic arch was collected at 0 weeks before modeling and at 2, 4, and 8 weeks after modeling to estimate blood vessel pressure. B-mode and M-mode ultrasound images were used to evaluate the left ventricular systolic function of the heart structure. The mitral valve flow Doppler combined with the mitral valve annular tissue Doppler was collected to evaluate the diastolic function of the heart, and the cardiac tissue was collected for histopathological observation.

  Results Ultrasound imaging results showed that aortic blood pressure increased significantly at 2, 4, and 8 weeks after surgery. Two weeks after operation, the main manifestations are the characteristic compensatory increase in thickness of left ventricular wall, decrease in inner diameter, and compensatory increase in systolic function, but it is accompanied by impaired diastolic function and myocardial fibrosis; 4 weeks after operation is a transition period, which is mainly manifested as Transition from ventricular wall hypertrophy to ventricular dilatation, systolic function began to decline, diastolic function continued to be damaged, and myocardium was further fibrotic; 8 weeks after operation, the characteristic ventricular cavity was enlarged, and both systolic and diastolic functions were significantly reduced. Cardiomyocytes were partially lysed and marked fibrosis.

  Conclusion By evaluating the left ventricular structure and function in three stages of compensatory myocardial hypertrophy, transition to decompensated dilated heart failure after aortic arch constriction in mice, the basic and translational research of aortic arch constriction model can be improved. The application provides a theoretical basis.